The International Forum on Consciousness offers a lively two days of information sharing and discussion regarding important—and often challenging—topics. Over the years, we have been guided through a range of topics, including creativity, near death, entheogens, intelligence in nature, business evolution and the effects of sensory inputs. This year, we’re tackling Means and Metrics for Detecting and Measuring Consciousness. You can find out more here: https://www.btci.org/events-symposia-2018/international-forum-on-consciousness/ .
As we work on the final details for this year and registrations flow in, I took a moment to pause and reflect on the fact that several of the registrants have joined us for many, if not all, of our past events. It’s gratifying to see that they are taking time out of their normal routines to make their way to the Promega campus again this spring. So, I asked a few of them to share their thoughts for this post and this is what they had to say: Continue reading
Image courtesy of Carlos Marti-Figueroa, Wisconsin Institute for Discovery, University of Wisconsin, Madison
On April 13th, the BTC Institute and Promega Corporation will host the 11th Annual Wisconsin Stem Cell Symposium — Stem Cells in the 4th Dimension: Mechanisms of Stem Cell Aging and Maturation.
Our co-coordinators at the UW-Madison Stem Cell and Regenerative Medicine Center have put together an outstanding list of presenters, including leading researchers who are investigating the effects of aging on stem cell populations and their progeny and recapitulating aging mechanisms in vitro to mature human stem cell derivatives and transplants.
The morning session will review systemic and cell autonomous factors known to impact stem cell maturation, aging and senescence. The afternoon session will focus on using these approaches and understanding to develop in vitro models of matured, stem cell-derived neural, cardiac, and pancreatic cells and tissues for regenerative medicine applications.
- Endocrine, micro-RNA, epigenetic, and metabolic regulators of aging
- Systemic regulators elucidated by parabiosis
- Treatment of age-related stem cell dysfunction
- In vivo and in vitro models of neural, musculoskeletal, cardiac, and pancreatic tissue maturation
Lewy Body stained with alpha-synuclein.
A week ago Sunday, I walked among crowds of mothers, grandmothers, and children of all ages celebrating Mother’s Day at the Botanical Gardens in St. Louis, Missouri. As I watched happy families, I couldn’t help being jealous. Though I was there with my grandmother and other close relatives, I missed my mom, especially since I was in my hometown for her funeral the day before. Had my mom been alive and well, we might have walked those same paths ourselves and enjoyed the new life teeming above the earth. Instead, my mother lost her battle of more than six years with Lewy Body dementia the week before at the age of 61.
As a biologist, I was well-aware of Alzheimer disease in the abstract, and tau proteins, beta-amyloid, and genetic predisposition. But until my mom was diagnosed in 2008, I was painfully ignorant of dementias other than Alzheimer disease. Once we knew what mom was fighting, I learned that Alzheimer disease and Lewy Body are hardly unique. The number of other dementias that exist is long and includes vascular dementia, mixed dementia, Parkinson’s disease, frontotemporal dementia, Creutzfeldt-Jakob disease, Huntington disease, and many others. Continue reading
We all know that a healthy lifestyle (diet high in whole foods and low in fat, moderate exercise, managing stress and good social support) is good for us. In fact I will go so far as to say that it isn’t even news that these things help our health and well-being. What is news, or at least newly published, is that these changes may also have a positive effect on telomerase activity and telomere length (1). Continue reading
If asked what are the differences between a grandfather and his newborn granddaughter, I would reply with the obvious ones: size (the grandfather is larger than his granddaughter), condition of the skin (babies have soft, smooth skin and elders have age spots and wrinkles) and life expectancy. Other visual cues may seem more similar than different. For example, grandfather and granddaughter may both lack hair on their heads or need assistance to move from one place to another. However, both baby and elder are a product of the genes expressed from their genome even if the exact sequence is not identical between them. Because genes are expressed differently over a human’s lifetime, Heyn et al. decided to examine the methylation profile in the genomes of newborns and individuals 89 years old or older. Continue reading
There are some things that science can tell me that I’m not sure I want to know. For example, I’m not sure I want to know the sequence of my own genome and my projected risk of developing any particular, currently incurable diseases. There are some things it is better not to know, particularly if there is nothing you can do about it anyway. Until recently I would have put telomere length into this category as well. Short telomeres are an indicator of biological age and are associated with increased susceptibility to diseases of aging. And stress, such as could be caused by worrying about how short your telomeres are, is known to make them even shorter. So why find out? It turns out that there are some things under our control that can positively affect telomere length.
Telomeres are nucleoprotein structures at the end of chromosomes that protect them from damage and ensure that genetic information is not lost during cell division. DNA polymerases cannot replicate DNA at the ends of chromosomes effectively, and without the protective effects of telomeres a small amount of chromosomal DNA would be lost with each cycle of cell division. The stretches of repetitive telomere DNA prevent progressive shortening of the chromosome, but are themselves shortened with each cell division. Telomere shortening limits the number of times that a cell can divide. Somatic cells are capable of a finite number of divisions, a number known as the Hayflick limit. Once cells reach that limit, they die. This limit is associated with telomere length. Once telomeres reach a critical length, cellular senescence is triggered, and a cell stops dividing and dies. Because of this, telomere length can act as a gauge of cellular or “biological” age. Continue reading
Add pomegranite to the list of so-called superfoods.
Since the 1980s, we’ve been told that aging can be accelerated by a build-up of free radicals in our cells. We’ve learned that to counteract the damage that free radicals (or reactive oxygen species, ROS) can wreak on our bodies, we should consume antioxidants like vitamins C and E, and phytochemicals.
In fact, the term “superfood” was coined for foods that contain high levels of antioxidants, phytochemicals and vitamins, foods like blueberries and carrots, spinach and kale, to name a few.
“Hold the phone”, as a pre-calculus professor of mine used to say. Turn off the blender and put down that shot glass of beet-carrot-lemon grass juice. This research just in: “Free Radicals Crucial to Suppressing Appetite”.
The research was published August 28, 2011 in the advanced online edition of Nature Medicine.
In this study, Yale University researchers reported that elevated levels of ROS in the brain activated satiety-generating neurons. Continue reading
Stories abound about the Spanish explorer Juan Ponce de Leon, who back in the 15th century searched in vain for the Fountain of Youth in what is now Florida (with some historians stating that he was actually looking for a solution to his own sexual impotence). In recent times, the magician David Copperfield has stated that he owns the Fountain of Youth, which is located on his Bahamas property. Copperfield claims that his Fountain of Youth actually brings animals that are close to death back to life. Stories about fountains, trees, and fruit with properties of everlasting youth have been in existence since the Babylonians composed the Epic of Gilgamesh. In modern times, scientists have purported that there is another source of youth and prolonged life: calorie restriction. Continue reading
I know that results in mice do not always translate to humans. I know that. I know that clinical trials can take years and that there are many hurdles between the first promising result in an animal model and the actual development of some form of treatment. Nevertheless I could not stifle a surge of hope when I heard about recent research suggesting that GM-CSF treatment reversed cognitive impairment and amyloid build-up in Alzheimer mice.
I have watched two family members succumb to Alzheimer’s disease. To me the news that something not only halted progression but actually reversed some of the cognitive impairment is huge. I know…its only in mice, but it’s the most promising news about this disease that I’ve heard in a while. And there’s more, the effective factor, GM-CSF, is already available in the drug Leukine, which is currently used to reduce risk of infection in cancer patients. Continue reading
[picapp align=”right” wrap=”false” link=”term=marathon&iid=8745671″ src=”9/f/a/5/Prague_International_Marathon_d037.jpg?adImageId=12882162&imageId=8745671″ width=”234″ height=”288″ /]On Saturday I ran 12 miles. “Well, at least I have staved off apoptosis in my peripheral blood mononuclear cells” I thought as I hobbled down the stairs on Sunday morning. Normally I don’t think about mononuclear cells on Sunday mornings, only of coffee. However, a paper published last week in BMC Physiology changed that for me, at least temporarily.
The paper, by Marfe et al, investigated whether the physiological stress associated with strenuous exercise may cause apoptosis and contribute to loss of lymphocytes. This paper investigated whether apoptosis is increased in cells of the immune system after running a marathon. The authors studied the expression of various stress-related proteins in peripheral blood lymphocytes in 10 male amateur runners, examining the expression of various antioxidants, stress proteins and apoptotic markers before and after (2-hours post-race) running a marathon. They found that expression of the apoptotic marker bax was decreased significantly after the marathon, while levels of antiapoptotic bcl-2 RNA increased. The amount of propcaspase 9 did not change pre and post race, indicating that there was no change in levels of apoptosis before and after the race. Continue reading